Diabetes is a disease in which the function of insulin becomes insufficient, the blood glucose level becomes high, and sugar is detected even in urine. Insulin is produced in and secreted from pancreatic β cells, promotes synthesis of glycogen (storage type glucose) from glucose in the liver and muscle, suppresses degradation of glycogen into glucose in the liver, and suppresses increase in the blood glucose level.
The number of patients is increasing mainly due to overeating, lack of exercise, obesity, stress, and genetic factors.
Diabetes is largely divided into type 1 diabetes showing absolute lack of insulin, and type 2 diabetes showing relative lack of insulin. Type 1 is basically treated with insulin injection, and type 2 is basically treated with diet and exercise therapy, though drug therapy is necessary when the blood glucose cannot be controlled well. For drug therapy, oral therapeutic drug for diabetes or insulin is used, both of which require improvement in terms of side effects, QOL and the like.
In addition, the condition developing lifestyle-related diseases such as hypertension, hyperlipidemia, diabetes and the like due to the accumulated visceral fat is referred to as metabolic syndrome, and has been widely recognized to increase the risk of developing arteriosclerotic diseases (myocardial infarction, cerebral infarction etc.). Accordingly, the prophylaxis or treatment of diabetes is necessarily effective for the prophylaxis or treatment of metabolic syndrome.
On the other hand, 8-[2-(2-pentyl-cyclopropylmethyl)-cyclopropyl]-octanoic acid (DCP-LA), which is a linoleic acid derivative, is a compound having a long-term enhancing action on synapse transmission efficiency, which can delay metabolism in the body and can maintain stable LTP (long-term potentiation)-like enhancement of synapse transmission (patent document 1).
Some reports have also been documented as regards DCP-LA. For example, it has been reported that DCP-LA activates PKC-ε selectively and directly (non-patent document 1), DCP-LA improves cognitive dysfunction of senescence accelerated mouse (non-patent document 2), DCP-LA increases release of γ aminobutyric acid from hippocampus nerve cells (non-patent document 3), DCP-LA improves cognitive dysfunction of amyloid β peptide or scopolamine-treated rat (non-patent document 4), and DCP-LA promotes hippocampal synaptic transmission with α7 nicotinic acetylcholine receptor expressed in glutamatergic presynaptic cell as a target (non-patent document 5). Furthermore, it has been reported in recent years that DCP-LA has an action to suppress nerve cell death induced by oxidative stress (patent document 2).